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A 73-year-old man presented with a thunderclap headache (TCH), suggesting a subarachnoid haemorrhage. Neurological examination, computer tomography of the head, and cerebrospinal fluid examination were normal. Magnetic resonance imaging of the brain revealed a supratentorial cerebral infarct. No cerebral aneurysm could be detected. A TCH can be the presenting feature of many conditions. A formula for the diagnostic assessment of TCH should be established. The management of this type of headache is controversial. Articles differ in their conclusions and recommendations. An expansion of routine investigations should be performed in cases where the neurological examination, cerebrospinal fluid analysis, and computer tomography are normal. A TCH can be the primary clinical feature of a supratentorial cerebral infarct.

Introduction Hypertensive encephalopathy with the clinicoradiological entity posterior reversible encephalopathy syndrome in the setting of venlafaxine as single therapy has not been reported earlier. Case description A 46-year-old man developed hypertensive encephalopathy associated with venlafaxine as single therapy. Magnetic resonance imaging of the brain, pre and post gadolinium, carried out on day 2, displayed an increased T2 signal in the cortex on both the T2 and FLAIR images throughout the frontal and temporal lobes and in the cerebellum. Venlafaxine therapy was stopped. The patient gradually improved and he became seizure free and the blood pressure successively became normal. A magnetic resonance imaging after six weeks displayed marked regression of the abnormalities. On follow-up after 3 months, his blood pressure had been normal and he had not had any symptoms. The prescribed antiepileptic drug was discontinued as well as antihypertensive treatment. He had not experienced any new symptoms at follow-up after one year. Discussion and evaluation The patient in this report had hypertensive encephalopathy associated with venlafaxine therapy. The imaging findings are compatible with hypertensive encephalopathy/posterior reversible encephalopathy syndrome. Venlafaxine is a drug used very frequently. Venlafaxine may infrequently induce hypertensive crisis. Conclusion Hypertensive encephalopathy may rarely occur in the setting of venlafaxine as single therapy even in low to moderate doses. Patients on venlafaxine should have regular monitoring of blood pressure. Knowledge of the side effects is vital. Venlafaxine must be discontinued if significant hypertension persists.

Introduction Hypertensive encephalopathy is one cause of posterior reversible encephalopathy syndrome. Hypertensive encephalopathy and cerebral infarction have only been reported in a few individual case reports. Case description A 51-year-old woman presented with hypertensive encephalopathy. T2-weighted images from magnetic resonance imaging showed hyperintense lesions in both occipital and parietal lobes. Diffusion-weighted imaging showed that this represented cytotoxic oedema and perfusion magnetic resonance imaging revealed reduced blood volume and flow. The magnetic resonance imaging was repeated 5 months later and subtotal regression of theT2-hyperintensity had occurred. However, small bilateral infarcts were seen on T1-weighted images. Perfusion magnetic resonance imaging presented reduced blood volume and flow on the right side. Discussion and evaluation The patient in this report had posterior reversible encephalopathy syndrome caused by hypertensive encephalopathy. Magnetic resonance imaging of the brain showed bilateral cytotoxic oedema that partially resolved and resulted in small infarcts. The imaging findings are compatible with posterior reversible encephalopathy syndrome with subtotal resolution and infarct evolution. Conclusion The case report suggests that the presence of hypertensive encephalopathy and posterior reversible encephalopathy syndrome should alert clinicians and lead to prompt treatment in order to prevent cerebral damage.

Background Chronic migraine (CM) is a type of chronic daily headache. CM presents a challenge to primary care physicians and neurologists. Any new treatment showing efficiency would therefore be of great importance. Atenolol together with other beta-blockers is a first-line choice in episodic migraine prophylaxis. Clinical findings support the efficacy of atenolol in doses of 50 to 200 mg/day. Methods Here I present an open-label study the aim of which is to evaluate the efficacy and tolerability of atenolol (50 mg o.d) for the prevention of CM. 19 patients affected by CM were studied. Results Following a one-month run-in period, the patients took atenolol for 3 months. Mean numbers of headache days per month were reduced from 20.1 ± 2.4 during the run-in period to 7.8 ± 6.1 by month 1.5 and to 7.1 ± 5.7 by the 3rd month of treatment (p < 0.0003). There was a significant difference between 1.5 months and the 3rd month (p < 0.006). The severity of attacks was reduced from a mean 2.3 ± 0.6 to 1.4 ± 1.1 (p < 0.010) at 1.5 months. In this, there was no difference between 1.5 months and the 3rd month. In 5 (29%) of the17 patients who completed the study, CM was totally gone during the 3rd month of treatment. No patient was totally unresponsive to the drug. Among the patients who completed the study, the treatment was well tolerated and the compliance was good. Conclusion Atenolol seems to be a safe and effective treatment for CM. Controlled trials are needed to confirm the observed results.

Background Cluster headache is a primary headache by definition not caused by any known underlying structural pathology. However, symptomatic cases have been described, for example tumours, particularly pituitary adenomas, malformations, and infections/inflammations. The evaluation of cluster headache is an issue unresolved. Case description I present a case of a 24-year-old patient who presented with a 4-week history of side-locked attacks of pain located in the left orbit. He satisfied the revised International Classification of Headache Disorders criteria for cluster headache. His medical and family histories were unremarkable. There was no history of headache. A diagnosis of cluster headache was made. The patient responded to symptomatic treatment. Low-dose computer tomography scan after 2 weeks displayed a left-sided acute maxillary sinusitis. The headache attacks resolved completely after treatment with antibiotics and sinus puncture. Discussion and evaluation Although I cannot exclude an unintentional comorbidity, in my opinion, the co-occurrence of an acute maxillary sinusitis with unilateral headache, in a hitherto headache-free man, points toward the fact that in this case the cluster headache was caused or triggered by the sinusitis. The headache attacks resolved completely after the treatment and the patient also remained headache free at the follow-up. The response of the headache to sumatriptan and other typical cluster headache medications does not exclude a secondary form. Symptomatic cluster headaches responsive to this therapy have been described. Associated cranial lesions such as infections have been reported in cluster headache patients and the attacks may be clinically indistinguishable from the primary form. Conclusions Neuroimaging, preferably contrast-enhanced magnetic resonance imaging including sinuses should always be considered in patients with cluster headache despite normal neurological examination. Acute maxillary sinusitis can present as cluster headache.

In the study by Gultekin [6] patients with anti-Ma2 antibodies were young men with testicular germ-cell tumors (100%) and with frequent hypothalamic involvement and a poor neurological outcome. [...] testicular carcinoma should be ruled out in younger men displaying a Ma2 paraneoplastic syndrome.

Background Cluster headache is a primary headache by definition not caused by any known underlying structural pathology. However, symptomatic cases have been described, e.g. tumours, particularly pituitary adenomas, malformations, and infections/inflammations. The evaluation of cluster headache is an issue unresolved. Case description We present a case of a 43-year-old patient who presented with a 2-month history of side-locked attacks of pain located in the left orbit. He satisfied the revised International Classification of Headache Disorders criteria for cluster headache. His medical and family histories were unremarkable. There was no history of headache. A diagnosis of cluster headache was made. The patient responded to symptomatic treatment. Computer tomography and enhanced magnetic resonance imaging after 1 month displayed a supra- and intrasellar arachnoid cyst with mass effect on adjacent structures. After operation, the headache attacks resolved completely. Discussion and evaluation Although we cannot exclude an unintentional comorbidity, in our opinion, the co-occurrence of an arachnoid cyst with mass effect with unilateral headache, in a hitherto headache-free man, points toward the fact that in this case the CH was caused or triggered by the AC. The headache attacks resolved completely after the operation and the patient also remained headache free at the follow-up. The response of the headache to sumatriptan and other typical CH medications does not exclude a secondary form. Symptomatic CHs responsive to this therapy have been described. Associated cranial lesions such as tumours have been reported in CH patients and the attacks may be clinically indistinguishable from the primary form. Conclusions Neuroimaging, preferably contrast-enhanced magnetic resonance imaging should always be considered in patients with cluster headache despite normal neurological examination. Late-onset cluster headache represents a condition that requires careful evaluation. Supra- and intrasellar arachnoid cyst can present as cluster headache.

A 32-year-old man with a residual spastic quadriparesis from a traumatic C5–C6 fracture experienced a severe thunderclap headache. The medical history revealed an episode of autonomic dysreflexia (AD) due to neurogenic bladder/urinary tract infection (UTI). Blood pressure monitoring at admission revealed hypertension; blood pressure reaching 160/100 mmHg (average blood pressure in these patients and also in this patient being 90/60 mmHg). CT scan of the head, cerebrospinal fluid examination, CT angiography and MR angiography of the brain vessels were normal. Another UTI and a subsequent spell of AD were diagnosed. The patient continued to experience recurrent thunderclap headaches. Selective catheter cerebral angiography revealed multiple calibre changes in the intracranial blood vessels. A diagnosis of reversible cerebral vasoconstriction syndrome (RCVS) due to AD was considered. A magnetic resonance imaging (MRI) of the brain after 2 weeks revealed ischaemic changes in the left hemisphere. Follow-up brain MRI after 3 weeks showed reduction in size of the ischaemic changes, and catheter angiography after 6 weeks demonstrated improvement/normalization. A diagnosis of RCVS could be established. Repeated MRI/CT of the brain after 6 months demonstrated a large infarction in the left hemisphere. RCVS has been reported to occur in various clinical settings. It can occur in the setting of AD in patients with traumatic cervical cord injury. Prompt recognition of RCVS may be of vital importance to avoid further morbidity in patients with spinal cord injury.

{Figure 1} The neurological complications described in association with intensive head banging include subdural hematoma, [2],[3] vertebral artery aneurysm, [4] carotid artery dissection, [5] whiplash injury, [6] odontoid fracture, [7] and vertebral artery dissection with vertebrobasilar ischemia or infarction. Vertebrobasilar ischemia or infarction as a result of extremes of cervical motion is probably due to the fact that the vertebral arteries are fixed in the transverse foramina, rendering them susceptible to occlusion or shearing from extremes of neck motion.